Search results for "Exons"

showing 10 items of 197 documents

A recurrent TP63 mutation causing EEC3 and Rapp–Hodgkin syndromes

2016

The ectrodactyly, ectodermal dysplasia, and cleft lip/palate syndrome 3 (EEC3; OMIM #604292), the Rapp-Hodgkin syndrome (RHS), and various other syndromes are caused by mutations in the TP63 gene, which encodes a p53-like transcription factor. Here, we report on a woman aged 37 years and her daughter aged 3 years with the previously reported c.1028G>A (p.Arg343Gln) mutation in exon 8 of TP63. The mother lacked ectrodactyly, indicating a diagnosis of RHS, whereas the girl presented with all three major features (ectrodactyly, ectodermal dysplasia, clefting) and different minor features (including small and brittle nails, and recurrent conjunctivitis believed to be because of stenotic and blo…

Adult0301 basic medicineHeterozygoteEctodermal dysplasiamedicine.medical_specialtyEctrodactylyFoot Deformities CongenitalCleft Lipmedia_common.quotation_subjectmedicine.disease_causePathology and Forensic MedicineFingers030207 dermatology & venereal diseases03 medical and health sciencesExon0302 clinical medicineEctodermal DysplasiaTP63medicineHumansAlleleAllelesGenetics (clinical)media_commonDaughterMutationbusiness.industryTumor Suppressor ProteinsFaciesExonsGeneral Medicinemedicine.diseaseDermatologyPenetrancePedigreeCleft PalatePhenotype030104 developmental biologyAmino Acid SubstitutionChild PreschoolMutationPediatrics Perinatology and Child HealthFemaleAnatomybusinessHand Deformities CongenitalTranscription FactorsClinical Dysmorphology
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iGEMS: an integrated model for identification of alternative exon usage events.

2016

Abstract DNA microarrays and RNAseq are complementary methods for studying RNA molecules. Current computational methods to determine alternative exon usage (AEU) using such data require impractical visual inspection and still yield high false-positive rates. Integrated Gene and Exon Model of Splicing (iGEMS) adapts a gene-level residuals model with a gene size adjusted false discovery rate and exon-level analysis to circumvent these limitations. iGEMS was applied to two new DNA microarray datasets, including the high coverage Human Transcriptome Arrays 2.0 and performance was validated using RT-qPCR. First, AEU was studied in adipocytes treated with (n = 9) or without (n = 8) the anti-diabe…

AdultAlternative SplicingMiceGene Expression ProfilingAnimalsComputational BiologyHumansMethods OnlineExonsGenomicsTranscriptomeOligonucleotide Array Sequence AnalysisNucleic acids research
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X-Linked Dilated Cardiomyopathy.

1995

We report on a family with a severe form of X-linked dilated cardiomyopathy (DCM). Two brothers, the elder requiring heart transplantation, and a maternal cousin presented elevated creatine kinase levels, increased right ventricular diameters and electrocardiographic abnormalities. All complained of exertional cramping myalgia, but none had muscle weakness or a pathological electromyogram. Muscle biopsies of these individuals revealed a mild myopathic picture with atrophic type I and hypertrophic type II fibers. Immunofluorescence using N- and C-terminal antibodies (dys-2, dys-3) against the dystrophin protein showed preserved, but reduced intensity of staining of the sarcolemmal membranes.…

AdultCardiomyopathy DilatedGenetic MarkersMaleX ChromosomeGenetic LinkageBiopsyMyosinsImmunofluorescencePolymerase Chain ReactionGeneral Biochemistry Genetics and Molecular BiologyDystrophinExonHistory and Philosophy of ScienceWestern blotmedicineHumansRNA MessengerMuscle SkeletalDNA PrimersSequence DeletionSouthern blotRecombination Geneticbiologymedicine.diagnostic_testMyocardiumGeneral NeuroscienceChromosome MappingDilated cardiomyopathyExonsmusculoskeletal systemmedicine.diseaseMolecular biologyPedigreeAlternative Splicingbiology.proteinFemaleCreatine kinaseLod ScoreAntibodyDystrophinAnnals of the New York Academy of Sciences
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A mutation in myotilin causes spheroid body myopathy

2005

Background: Spheroid body myopathy (SBM) is a rare, autosomal dominant, neuromuscular disorder, which has only been previously reported in a single large kindred. Identification of the mutated gene in this disorder may provide insight regarding abnormal neuromuscular function. Methods: The authors completed a detailed clinical evaluation on an extensive kindred diagnosed with SBM. Genome-wide linkage analysis was performed to localize the disease gene to a specific chromosomal region. Further marker genotyping and screening of a positional, functional candidate gene were completed to detect the disease-causing mutation. Pathologic analysis of muscle biopsy was performed on three individuals…

AdultGenetic MarkersMaleCandidate genePathologymedicine.medical_specialtyDNA Mutational AnalysisMuscle ProteinsChromosome DisordersBiologyExonMuscular DiseasesmedicineHumansPoint MutationMyotilinConnectinGenetic Predisposition to DiseaseGenetic TestingMuscular dystrophyMuscle SkeletalMyopathyAgedGenes DominantAged 80 and overInclusion BodiesGeneticsMuscle biopsymedicine.diagnostic_testMicrofilament ProteinsChromosome MappingExonsMiddle Agedmedicine.diseasePedigreeCytoskeletal ProteinsMutationChromosomal regionbiology.proteinChromosomes Human Pair 5FemaleTitinNeurology (clinical)medicine.symptomNeurology
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Methylation of the oxytocin receptor gene in clinically depressed patients compared to controls: The role of OXTR rs53576 genotype

2015

The emerging field of epigenetics provides a biological basis for gene-environment interactions relevant to depression. We focus on DNA methylation of exon 1 and 2 of the oxytocin receptor gene (OXTR) promoter. The research aims of the current study were to compare OXTR DNA methylation of depressed patients with healthy control subjects and to investigate possible influences of the OXTR rs53576 genotype. The sample of the present study consisted of 43 clinically depressed women recruited from a psychosomatic inpatient unit and 42 healthy, female control subjects - mean age 30 years (SD = 9). DNA methylation profiles of the OXTR gene were assessed from leukocyte DNA by means of bisulfite seq…

AdultGenotypeBisulfite sequencingOXTRPoison controlOxytocinPolymorphism Single NucleotideMethylationExonGenotypeMedicineHumansEpigeneticsBiological PsychiatryGeneticsbusiness.industryDepressionMethylationExonsDNA MethylationMiddle AgedOxytocin receptorPsychiatry and Mental healthReceptors OxytocinDNA methylationLinear ModelsExon-specificFemalebusinessBiomarkers
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Not All Floating-Harbor Syndrome Cases are Due to Mutations in Exon 34 of SRCAP

2013

International audience; Floating-Harbor syndrome (FHS) is a rare disorder characterized by short stature, delayed bone age, speech delay, and dysmorphic facial features. We report here the molecular analysis of nine cases, fulfilling the diagnostic criteria for FHS. Using exome sequencing, we identified SRCAP as the disease gene in two cases and subsequently found SRCAP truncating mutations in 6/9 cases. All mutations occurred de novo and were located in exon 34, in accordance with the recent report of Hood et al. However, the absence of SRCAP mutations in 3/9 cases supported genetic heterogeneity of FH syndrome. Importantly, no major clinical differences were observed supporting clinical h…

AdultHeart Septal Defects VentricularMaleDNA Mutational AnalysisBiologyShort statureCraniofacial Abnormalitiesgenetic heterogeneity03 medical and health sciencesExonGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildFloating-Harbor syndromeGenetics (clinical)Exome sequencingGrowth Disorders030304 developmental biologyDisease geneGeneticsAdenosine Triphosphatases0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsGenetic heterogeneity030305 genetics & heredityBone ageExonsmedicine.diseaseSRCAP3. Good healthFloating–Harbor syndromeSpeech delayMutationFemalemedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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The autoantigen La/SS-B: Analysis of the expression of alternatively spliced La mRNA isoforms

1996

The gene for the nuclear autoantigen La/SS-B encodes two La mRNA isoforms. In order to study the function and expression of both La mRNA forms, an in situ hybridization procedure was developed allowing the selective identification of either exon 1 or exon 1'. For this purpose, digoxigenin-labeled exon-specific sense and anti-sense probes were prepared by in vitro transcription from plasmids that contained the respective exon sequence. Detection of the probes was carried out by using rhodamine-conjugated anti-digoxigenin antibody and confocal laser scanning microscopy. Both La mRNAs were found in the cytoplasm of endothelial cells but not in smooth muscle cells. In addition to the in situ te…

AdultHistologyMolecular Sequence DataGene ExpressionIn situ hybridizationBiologyAutoantigensPolymerase Chain ReactionPathology and Forensic MedicineExonExon trappingIsomerismGene expressionHumansSaphenous VeinEndotheliumRNA MessengerMammary ArteriesGeneIn Situ HybridizationMessenger RNABase SequenceExonsCell BiologyMolecular biologyAlternative SplicingLiverRibonucleoproteinsCytoplasmPrimer (molecular biology)DNA ProbesTranscription Factors
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A constitutive BCL2 down-regulation aggravates the phenotype of PKD1-mutant-induced polycystic kidney disease

2017

IF 5.340; International audience; The main identified function of BCL2 protein is to prevent cell death by apoptosis. Mice knock-out for Bcl2 demonstrate growth retardation, severe polycystic kidney disease (PKD), gray hair and lymphopenia, and die prematurely after birth. Here, we report a 40-year-old male referred to for abdominal and thoracic aortic dissection with associated aortic root aneurysm, PKD, lymphocytopenia with a history of T cell lymphoblastic lymphoma, white hair since the age of 20, and learning difficulties. PKD, which was also detected in the father and sister, was related to an inherited PKD1 mutation. The combination of PKD with gray hair and lymphocytopenia was also r…

AdultMale0301 basic medicineTRPP Cation Channelsphenotypebcl2 geneBiologymicro rnaMice03 medical and health sciencesdown-regulationsymptom aggravating factorshemic and lymphatic diseasest-lymphocyteGene expressionGeneticsmedicinePolycystic kidney diseaseAnimalsHumansGenetic Predisposition to Disease[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsgenesMolecular BiologyGeneGenetics (clinical)Exome sequencingMice KnockoutPKD1apoptosisExonsGeneral MedicinePolycystic Kidney Autosomal Dominantmedicine.diseasePhenotypePedigreeUp-Regulation3. Good healthMicroRNAs030104 developmental biologyMRNA SequencingProto-Oncogene Proteins c-bcl-2[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsImmunologyCancer researchLymphocytopeniapolycystic kidney diseasesbcl-2 proteinHuman Molecular Genetics
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Mutation spectrum and clinical investigation of achromatopsia patients with mutations in the GNAT2 gene

2019

Achromatopsia (ACHM) is a hereditary cone photoreceptor disorder characterized by the inability to discriminate colors, nystagmus, photophobia, and low-visual acuity. Six genes have been associated with this rare autosomal recessively inherited disease, including the GNAT2 gene encoding the catalytic α-subunit of the G-protein transducin which is expressed in the cone photoreceptor outer segment. Out of a cohort of 1,116 independent families diagnosed with a primary clinical diagnosis of ACHM, we identified 23 patients with ACHM from 19 independent families with likely causative mutations in GNAT2, representing 1.7% of our large ACHM cohort. In total 22 different potentially disease-causing…

AdultMaleAchromatopsiagenetic structuresAdolescentChild preschoolDNA Copy Number VariationsColor Vision DefectsBiologymedicine.disease_causeHeterotrimeric GTP-Binding Proteins/genetics03 medical and health sciencesExonGene duplicationGeneticsmedicineHumansGenetic Predisposition to DiseaseCopy-number variationColor Vision Defects/geneticsChildGenetics (clinical)030304 developmental biologyAgedGenetics0303 health sciencesGNAT2MutationSettore MED/30 - Malattie Apparato Visivo030305 genetics & heredityBreakpointInfantSequence Analysis DNAExonsMiddle Agedmedicine.diseaseHeterotrimeric GTP-Binding ProteinsPhotoreceptor outer segmenteye diseasesPedigreeSettore BIO/18 - GeneticaSequence Analysis DNA/methodsyoung adultFemalesense organsachromatopsia copy number variations GNAT2 mutations transducinmutation
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FUS mutations in sporadic amyotrophic lateral sclerosis

2011

Mutations in the FUS gene have recently been described as a cause of familial amyotrophic lateral sclerosis (ALS), but their role in the pathogenesis of sporadic ALS is unclear. We undertook mutational screening of all coding exons of FUS in 228 sporadic ALS cases, and, as previous reports suggest that exon 15 represents a mutational hotspot, we sequenced this exon in an additional 1295 sporadic cases. Six variants in six different cases were found, indicating that FUS mutations can underlie apparently sporadic ALS, but account for less than 1% of this form of disease. © 2010 .

AdultMaleAgingAmyotrophic lateral sclerosis; FUS; Italy; Sporadic disease; United States of America;AdolescentGenotypesporadic patientsDNA Mutational AnalysisALS; FUS mutations; sporadic patientsBiologymedicine.disease_causeArticlePathogenesisExonYoung AdultDNA Mutational AnalysisGenotypemedicineHumansFUS mutationsAmyotrophic lateral sclerosisChildGeneAgedGeneticsAged 80 and overMutationGeneral NeuroscienceAmyotrophic Lateral Sclerosisamyotrophic lateral sclerosis FUS geneticsExonsMiddle Agedmedicine.diseaseUnited StatesSettore MED/26 - NEUROLOGIAItalyMutationRNA-Binding Protein FUSFemaleNeurology (clinical)Geriatrics and GerontologyALSDevelopmental BiologyRNA-Binding Protein FUS
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